ABSTRACT
Objectives: Until recently, systemic opioids have been standard care for acute pain management of geriatric hip fracture; however, opioids increase risk for delirium. Fascia Iliaca compartment blocks (FICB) may be favored to systemic analgesia for reducing delirium, but this has not been well demonstrated. We evaluated the efficacy of adjunctive FICB versus systemic analgesia on delirium incidence, opioid consumption, and pain scores. Methods: This prospective, observational cohort study was performed in patients (55-90 years) with traumatic hip fracture admitted to five trauma centers within 12 hours of injury, enrolled between January 2019 and November 2020. The primary end point was development of delirium, defined by the Confusion Assessment Method tool, from arrival through 48 hours postoperatively, and analyzed with multivariate Firth logistic regression. Secondary end points were analyzed with analysis of covariance models and included preoperative and postoperative oral morphine equivalents and pain numeric rating scale scores. Results: There were 517 patients enrolled, 381 (74%) received FICB and 136 (26%) did not. Delirium incidence was 5.4% (n=28) and was similar for patients receiving FICB versus no FICB (FICB, 5.8% and no FICB, 4.4%; adjusted OR: 1.2 (95% CI 0.5 to 3.0), p=0.65). Opioid requirements were similar for patients receiving FICB and no FICB, preoperatively (p=0.75) and postoperatively (p=0.51). Pain scores were significantly lower with FICB than no FICB, preoperatively (4.2 vs 5.1, p=0.002) and postoperatively (2.9 vs 3.5, p=0.04). Conclusions: FICB demonstrated significant benefit on self-reported pain but without a concomitant reduction in opioid consumption. Regarding delirium incidence, these findings suggest clinical equipoise and the need for a randomized trial. Level of evidence: II-prospective, therapeutic.
ABSTRACT
Oxidative stress exacerbates brain damage following ischemia-reperfusion and traumatic brain injury (TBI). Management of TBI and critically ill patients commonly involves use of propofol, a sedation medication that acts as a general anesthetic with inherent antioxidant properties. Here we review available evidence from animal model systems and clinical studies that propofol protects against ischemia-reperfusion injury. However, evidence of propofol toxicity in humans exists and manifests as a rare complication, "propofol infusion syndrome" (PRIS). Evidence in animal models suggests that brain injury induces expression of the p75 neurotrophin receptor (p75NTR), which is associated with proapoptotic signaling. p75NTR-mediated apoptosis of neurons is further exacerbated by propofol's superinduction of p75NTR and concomitant inhibition of neurotrophin processing. Propofol is toxic to neurons but not astrocytes, a type of glial cell. Evidence suggests that propofol protects astrocytes from oxidative stress and stimulates astroglial-mediated protection of neurons. One may speculate that in brain injury patients under sedation/anesthesia, propofol provides brain tissue protection or aids in recovery by enhancing astrocyte function. Nevertheless, our understanding of neurologic recovery versus long-term neurological sequelae leading to neurodegeneration is poor, and it is also conceivable that propofol plays a partial as yet unrecognized role in long-term impairment of the injured brain.
